Download Apoptosis (Programmed Cell Death) and

anism.
37
Tox Appi
Haslett
C,
RAF,
Hanson
Wound
SJ,
Ross
Am J Pathol
Leslie
CC,
Respir
CC,
growth
The
1975;
Dis
York:
role
Plenum
of the
Clark
n
Biology
Publishing
of
Cor-
factors
K, Cook
JL,
in rat alveolar
DNA
synthesis
132:1246-52
DNA
Mol
ml
were
12.9%
type
Mac-
II cells.
RJ. Heparin-binding
in rat alveolar
synthesis
Biol
RJ.
1990;
25.9%±4.5%
± 2.9%
Similar
which
type
and
are
present
II
We
M.D.;
A. Lee, M.D.;
M.D.;
Despite
and
the
before
alternative
from
ptosis,
which
senescent
described
blood
or
the
stimulate
mediators.
effect
of
apoptosis
control
N.’
via
number
of
with
populations
have
shape
change,
but there
was
nonapoptotic
to the
apoptosis
may
also
proinflammatory
senting
an
contents
inflammatory
agents
rate
to
in
in
pure
were
inhibit,
of PMN
aggregation
or
exclusion).
For
in
loss
vitro
13
mersmith
6S
the Respiratory
Hospital,
Division,
London,
h in
Department
England.
is
cell
PMN
a
modulatable
contents,
leads
without
the
products,
disposal
to
mac-
release
of
thus
repre-
mechanism
impor-
83:865-75
343:170-73
by
programmed
This
leads
mechanism
M.D.
PMN
trypan
blue
resolving
to
recognition
cell
of intact
senescent
site
or apoptosis
inflamed
death
of
the
vitronectin
the
possible
of PMN
in the
aged
clear-
is determined
which
aging
PMN
by macrophages
adhesion
signal
the
neutrophils
mechanism
important
as
PMN.’
“senescent
via a mechanism
and a macrophage
receptor
(VnR),
sugars
ties
of activated
and
sought
play
in
critical
major
80%,
indicating
ml
in the
that
PMN
enhanced
and
TSP
the
aged
acts
of aged
we
with
of aged
maneuver)
mechanism.
Indeed,
TSP
on
there
the
a
was
between
in solution
whether
TSP
PMNs
played
bridge”
(1)
ad-
structures
this
uptake,
secrete
CD36,
coated
TSP-binding
as a “molecular
PMN
to
proper-
PMNs.
recognition
macrophage:
by
known
both
include
surfaces
by
recognition
PMNs
intercellular
to
that
specific
adhesive
which
recognition
(downregulated
evidence
aged
macrophages
subsequent
cell-
by
molecules
of TSP/CD36-mediated
inhibited
role
aged
Since
of macrophages
macrophage
of
acids,
for TSP,
in macrophage
specifically
additional
of
suggested
(TSP)-dependent
receptors
evidence
over
amino
platelets.
bear
Attachment
by
involvement
and basic
thrombospondin
amino
hesion
in
fashion,
(by
Haslett,
signaling
mechanisms
was
of macrophage
phagocytosis
inhibition
When
aging
the
However,
that
culture,
Chris
phagocytosis
is an
13:, integrin,
suggested
causing
and
self” and phagocytosis
which
the Arg-Gly-Asp
TSP
PMNs
Hogg,
acrophage
the
at 5 s.g/
in solution
in
the
untreated
*From
5From
of inflamma-
resolution.
Nancy
from
to be
without
integrity
after
at sites
macrophage
1989;
1990;
surface
(LPS),
granulocyte-mac(GM-CSF),
and chemotaccounterpart
FMLP
were
of membrane
example,
Invest
Savill,
appeared
removal.
with
John
inhibit
a concentration-dependent
in
was
apoptosis
Macrophage
Vitronectin
Receptor,
CD36, and Thrombospondin
Cooperate
in Recognition
of
Neutrophils
Undergoing
Programmed
Cell Death*
were
and
packaging
included
apoptosis
± 0.9%
roles.
included
stimulated
aged PMNs
into apoptotic
to macrophage
vitro,
bacterial
lipopolysaccharide
rophage
colony-stimulating
factor
t/c peptide
C5a and its synthetic
the
the
declined
which
as an “inert”
prior
of
apoptosis
intact
injury-limiting
in inflammatory
ance
for
cells
loss
fraction,
serve
for neutrophil
all found
functions
functional
apoptotic
rate
PMN
of the
(PMNs)
PMNs
and the
rate
of PMN
apoptotic
exclusion.
When
centrifugation
subpopulations,
restricted
appear
and stimulated
release
of granule
enzymes,
no evidence
of loss of membrane
integrity
as
by trypan
blue
by counterflow
PMN
“packaging”
further
M
apoptotic
not
implications
of
the
were
6.1%
intact
proinflammatory
of aging
on the
PMN
appearance
apo-
the
of
does
release
important
PMNs,
of
of PM Ns aging in vitro.
These
functions
phagocytosis
of opsonized
zymosan,
chemotaxis,
assessed
separated
undergo
that
properties
mediators
important
the
aging
sites,
recognition
to
in
concentration
that
by
removal
1 J Clin
(PMN)
which
ingestion
macrophage
would
also
of inflammation.
concert
by
mechanisms
The functional
inflammatory
neutrophil
inflamed
Macrophage
a novel
in high
that,
2 Nature
sites is poorly
underthat PMNs
inevitably
local macrophages,
an
by
from
1 ig/ml
were
M.D.;
of
to macrophage
leads
occurs
A
removal
been
PM
PMNs
to
their
has
fate
derived
potential
fate at inflamed
it is widely
assumed
Although
at
g/ml
REFERENCES
in
M.D.
their
disintegrate
10
at
Mediators
j S. Savill,
K. Whyte,
injurious
contents,
stood.
M.
at
reductions
hypothesize
process
Apoptosis
(Programmed
Cell
Death) and Functional
Changes
Aging Neutrophils*
L. Meagher,
LPS
with GM-CSF,
C5a,
and
FMLP,
that
the process
of apoptosis
can
be
PMN
longevity
can be prolonged
by factors
suggested
tant
C. Haslett,
and
± SE;
100 ng/
(mean
with
tion.
2:99-106
by Inflammatory
apoptotic
treated
treatment
modulated
rophage
Modulation
± 4.8%
apoptotic,
apoptotic,
following
that
K, Mason
stimulate
Mason
were
cell
apoptotic.
in wound
78:71-91
1985;
Cell
macrophage
43.3%
populations
populations
7) whereas
=
seen
McCormick-Shannon
Am J Respir
cells.
In:
and Cellular
Molecular
7. New
B.
stimulate
Rev
Leslie
PMN
of inflammation.
McCormick-Shannon
rophages
40
The
eds.
Chapter
repair.
Am
51:475-87
Resolution
1988:185-211
Leibovich
39
1979;
PM.
PM,
Repair,
poration,
38
Pharm
Hanson
of Medicine,
Ham-
School
(N.H.),
the
Department
of Medicine,
(IS.,
C.H.).
and
London,
England.
33rd
the
Annual
Imperial
Thomas
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